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中文摘要：
在探索脓毒症的发病机制中，人们已经认识到早期炎症因子肿瘤坏死因子-α（TNF-α）、白细胞介素-1（IL-1）在脓毒症的病理过程中具有重要作用，但应用TNF—α或IL-1拮抗剂干预并没有明显改善脓毒症患者的预后。其原因是多方面的，但主要与TNF-α的早期迅速合成、释放以及临床很难做到早期或预防性干预有关。另有资料表明，用致死剂量的内毒素攻击小鼠，部分动物5d后才死亡，而此时TNF-α、IL-1水平已降至正常范围；给TNF-α基因缺陷的小鼠注入内毒素数日后亦可导致死亡，这说明可能存在某些重要的晚期炎症介质介导了内毒素的致死效应。晚近研究发现，
英文摘要：
Objective To investigate the potential effect of high mobility group box 1 protein （HMGB1） on host immune response and its molecular regulation mechanism as well as its interventional pathway following major burns/trauma. Methods With both animal experiments and clinical investigation, serial studies were conducted to observe the effects of HMGB1 on changes in immune function of T lymphocytes, dendritic cells, and macrophages both in vivo and in vitro. Results It was found that thermal injury or trauma induced a delayed and persistent increase in HMGB1 expression as well as its release in various tissues. HMGB1 formation could markedly influence the cell-mediated immunity, including the changes in T lymphocytes, dendritic cells, and macrophages following major trauma or burns. These effects were closely related with dysfunction of various organs in the course of sepsis. Conclusion These data proved that HMGB1 not only acts as a novel ＂late＂ inflammatory mediator but is also closely associated with immunosuppression after acute insults. HMGB1 might play an important role in inducing systemic inflammatory response together with host immunological dissonance, resulting in the development of septic complications. Intervention of HMGB1 expression and release presumably provides a potentially effective way to regulate both excessive inflammatory and immune response, thereby as a measure to improve the prognosis of severe sepsis secondary to major trauma.
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